title: The negative influence of high-glucose ambience on neurogenesis in developing quail embryos.
abstract: Gestational diabetes is defined as glucose intolerance during pregnancy and it is presented as high blood glucose levels during the onset pregnancy. This condition has an adverse impact on fetal development but the mechanism involved is still not fully understood. In this study, we investigated the effects of high glucose on the developing quail embryo, especially its impact on the development of the nervous system. We established that high glucose altered the central nervous system mophologically, such that neural tube defects (NTDs) developed. In addition, we found that high glucose impaired nerve differentiation at dorsal root ganglia and in the developing limb buds, as revealed by neurofilament (NF) immunofluorescent staining. The dorsal root ganglia are normally derived from neural crest cells (NCCs), so we examine the delamination of NCCs from dorsal side of the neural tube. We established that high glucose was detrimental to the NCCs, in vivo and in vitro. High glucose also negatively affected neural differentiation by reducing the number and length of neurites emanating from neurons in culture. We established that high glucose exposure caused an increase in reactive oxidative species (ROS) generation by primary cultured neurons. We hypothesized that excess ROS was the factor responsible for impairing neuron development and differentiation. We provided evidence for our hypothesis by showing that the addition of vitamin C (a powerful antioxidant) could rescue the damaging effects of high glucose on cultured neurons.
authors.affiliation: Key Laboratory for Regenerative Medicine of the Ministry of Education, Division of Histology and Embryology, Medical College, Jinan University, Guangzhou, China.
authors.forename: Yao
authors.initials: Y
authors.lastname: Chen
authors.forename: Jian-xia
authors.initials: JX
authors.lastname: Fan
authors.forename: Zhao-long
authors.initials: ZL
authors.lastname: Zhang
authors.forename: Guang
authors.initials: G
authors.lastname: Wang
authors.forename: Xin
authors.initials: X
authors.lastname: Cheng
authors.forename: Manli
authors.initials: M
authors.lastname: Chuai
authors.forename: Kenneth Ka Ho
authors.initials: KK
authors.lastname: Lee
authors.forename: Xuesong
authors.initials: X
authors.lastname: Yang
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D002490:Central Nervous System / Q000166:cytology / Q000187:drug effects / Q000196:embryology; D004305:Dose-Response Relationship, Drug; D005260:Female; D005727:Ganglia, Spinal / Q000166:cytology / Q000187:drug effects / Q000196:embryology; D005947:Glucose / Q000494:pharmacology* / Q000633:toxicity; D009420:Nervous System / Q000166:cytology / Q000187:drug effects* / Q000196:embryology; D009432:Neural Crest / Q000166:cytology / Q000187:drug effects / Q000196:embryology; D009436:Neural Tube Defects / Q000139:chemically induced; D016501:Neurites / Q000187:drug effects / Q000502:physiology; D055495:Neurogenesis / Q000187:drug effects*; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D011784:Quail / Q000196:embryology*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D005947:Glucose